Poster abstracts

Poster number 113 submitted by Emily Susa

Mitochondrial gene expression responds to lack of nutrients but not to different nutrient sources in Trypanosoma cruzi

Emily K. Susa (Biomedical Sciences, University of Minnesota Medical School, Duluth campus), Sara L. Zimmer (Biomedical Sciences, University of Minnesota Medical School, Duluth campus)

Abstract:
Trypanosoma cruzi is a vector-borne protozoan parasite that causes Chagas’ disease. The parasite has a complex life cycle which involves a variety of different environments and nutrient sources. In the midgut of the insect vector, glucose and amino acids are available to T. cruzi, but these resources dwindle over time and prompt differentiation into a nonreplicative but highly infective life stage. Upon contact with a host, T. cruzi invades mammalian cells and resumes replication, likely utilizing fatty acids for energy. To better understand the complicated relationship between nutrient source, metabolism and life stage differentiation, we are examining changes in the T. cruzi mitochondrial genome within different life stages. We are interested in the mitochondrial genome because of its roles in metabolism and because it exhibits life-stage specific remodeling in related species. Mitochondrial genome regulation must occur post-transcriptionally in the form of RNA editing, translational control, and stability. Previously, we examined mRNA transcript abundance between the insect midgut (epimastigote) stage and the insect hindgut (metacyclic trypomastigote) stage. Significant changes were detected in mature mRNA abundance between these life stages, but the differences appeared to have a stronger connection with the process of starvation than with the process of differentiation. We now examine mitochondrial transcript abundance in the intracellular (amastigote) stage. Expression is similar to that of actively dividing epimastigotes, and different from the starved population used to infect the mammalian cultures, with RNA editing as well as turnover appearing to be the cause of the differences. Our results indicate that environmental nutrient depletion rather than predominant source of energy is the major stimulus for changes to mitochondrial gene expression across the life cycle.

Keywords: mitochondria, editing, Trypanosoma cruzi